US7404221B2 - Reciprocating movement platform for the external addition of pulses to the fluid channels of a subject - Google Patents

Reciprocating movement platform for the external addition of pulses to the fluid channels of a subject Download PDF

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US7404221B2
US7404221B2 US10/566,872 US56687204A US7404221B2 US 7404221 B2 US7404221 B2 US 7404221B2 US 56687204 A US56687204 A US 56687204A US 7404221 B2 US7404221 B2 US 7404221B2
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periodic acceleration
motion platform
subject
acceleration
periodic
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US20060185083A1 (en
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Marvin A. Sackner
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Non-Invasive Monitoring Systems Inc
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Non-Invasive Monitoring Systems Inc
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    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61H—PHYSICAL THERAPY APPARATUS, e.g. DEVICES FOR LOCATING OR STIMULATING REFLEX POINTS IN THE BODY; ARTIFICIAL RESPIRATION; MASSAGE; BATHING DEVICES FOR SPECIAL THERAPEUTIC OR HYGIENIC PURPOSES OR SPECIFIC PARTS OF THE BODY
    • A61H1/00—Apparatus for passive exercising; Vibrating apparatus; Chiropractic devices, e.g. body impacting devices, external devices for briefly extending or aligning unbroken bones
    • A61H1/006—Apparatus for applying pressure or blows for compressive stressing of a part of the skeletal structure, e.g. for preventing or alleviating osteoporosis
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61G—TRANSPORT, PERSONAL CONVEYANCES, OR ACCOMMODATION SPECIALLY ADAPTED FOR PATIENTS OR DISABLED PERSONS; OPERATING TABLES OR CHAIRS; CHAIRS FOR DENTISTRY; FUNERAL DEVICES
    • A61G7/00—Beds specially adapted for nursing; Devices for lifting patients or disabled persons
    • A61G7/05—Parts, details or accessories of beds
    • A61G7/057—Arrangements for preventing bed-sores or for supporting patients with burns, e.g. mattresses specially adapted therefor
    • A61G7/0573—Arrangements for preventing bed-sores or for supporting patients with burns, e.g. mattresses specially adapted therefor with mattress frames having alternately movable parts
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61H—PHYSICAL THERAPY APPARATUS, e.g. DEVICES FOR LOCATING OR STIMULATING REFLEX POINTS IN THE BODY; ARTIFICIAL RESPIRATION; MASSAGE; BATHING DEVICES FOR SPECIAL THERAPEUTIC OR HYGIENIC PURPOSES OR SPECIFIC PARTS OF THE BODY
    • A61H2201/00—Characteristics of apparatus not provided for in the preceding codes
    • A61H2201/01—Constructive details
    • A61H2201/0119—Support for the device
    • A61H2201/0138—Support for the device incorporated in furniture
    • A61H2201/0142—Beds
    • A—HUMAN NECESSITIES
    • A61—MEDICAL OR VETERINARY SCIENCE; HYGIENE
    • A61H—PHYSICAL THERAPY APPARATUS, e.g. DEVICES FOR LOCATING OR STIMULATING REFLEX POINTS IN THE BODY; ARTIFICIAL RESPIRATION; MASSAGE; BATHING DEVICES FOR SPECIAL THERAPEUTIC OR HYGIENIC PURPOSES OR SPECIFIC PARTS OF THE BODY
    • A61H2203/00—Additional characteristics concerning the patient
    • A61H2203/04—Position of the patient
    • A61H2203/0443—Position of the patient substantially horizontal
    • A61H2203/0456—Supine

Definitions

  • the present invention relates generally to a reciprocating motion platform for oscillating a subject in a back and forth, headward to footward manner in order to externally add pulses to the fluid channels of the subject.
  • the external addition of pulses caused by the periodic acceleration of the subject results in many therapeutic benefits.
  • FIGS. 1 , 4 , 5 , and 6 show a completely constructed reciprocating movement platform comprised of a mattress 101 for the subject to lie upon, a pillow 102 for the subject's head, a footboard frame 103 with cast shoes 104 attached in order to secure the subject, a mattress support 105 to hold the mattress 101 and to which the footboard frame 103 is attached, a box frame 800 which holds the drive machinery (or “drive”) 200 onto which the mattress support 105 is attached, bumpers 820 attached to the top and bottom of the box frame 800 , and casters 830 at the four corners of the bottom of the box frame 800 for moving the reciprocating movement platform.
  • drive or “drive”
  • the entire reciprocating movement platform system (without patient, i.e., mattress 101 and mattress support 105 , footboard support 105 , box frame 800 , and drive machinery 200 ) weighs between 400 and 500 lbs.
  • the entire reciprocating movement platform system is 30′′ wide, which is the standard width of a hospital gurney, so that it may be easily moved through doorways, semi-crowded offices, etc.
  • the length of the entire system from bumper to bumper is 88′′, which is as long as a standard twin or king size bed.
  • the mattress 101 is 30′′ above the floor, and the top of the footboard support 103 is 42′′ above the floor.
  • the mattress support 105 secures the mattress 101 by means of Velcro strips.
  • the mattress support 105 and footboard support 105 together weigh roughly 120 lbs. total. When assembled, the combined mattress support 105 and footboard support 105 are 30′′ wide and 82′′ long.
  • the mattress 101 is 6′′ thick, 30′′ wide, 80′′ long, and weighs approximately 30 lbs.
  • the top 3′′ of the mattress foam is the “visco-elastic” type foam for form-fitting comfort while the subject is on the platform.
  • the mattress 101 can be designed to fold in half for easier transport and storage.
  • FIG. 7 shows the cast shoes 104 and the footboard frame 103 to which they are attached.
  • the cast shoes 104 of the footboard frame 103 are the only means by which the subject is secured to the mattress support 105 , and thus, is the means by which the subject is “pulsed” by the reciprocating platform.
  • the two cast shoes 104 are rigidly attached by nuts and bolts to the footboard frame 103 .
  • Once the subject is lying on the mattress 101 he or she will put his or her feet (with shoes on) into the cast shoes 104 and then the cast shoes 104 will be secured around the shoes by a system of Velcro and straps and cloth.
  • the feet may be fastened in the cast shoes 104 by other means, such as a ski boot-like apparatus, or another fastening means, such as a snap, a buckle, a lock, etc. connection.
  • the casters 830 on the bottom portion of the reciprocating movement platform are 6′′ hospital bed casters with central locking features; these provide easy rolling and maneuvering, good ground clearance, easy locking (as shown by the brake petal), and an attractive appearance.
  • the ground clearance is approximately 8′′, which accommodates the use of equipment (such as hoists) to lift the reciprocating movement platform.
  • the bumpers 820 make sure the reciprocating platform is not set too close to a wall by extending further out than the mattress support 105 .
  • the mattress support 105 is 82′′ long and, when the platform is engaged in a reciprocating movement, has a range of movement of +/ ⁇ 2′′.
  • the bumpers 820 are built to extend 1′′ beyond the furthest limit the mattress support 105 can travel so that the reciprocating movement platform will not be accidentally set too close to a wall where it might bump the wall during operation.
  • the drive machinery (or “drive”) 200 is enclosed within the box frame 800 and, as such, cannot be seen from the outside of the fully assembled movement platform. Supported by the box frame 800 and attached to the mattress support 105 , the drive 200 provides the reciprocating movement of the device.
  • the reciprocating (headwards-footwards) movement preferably has a rate of about 120-180 rpm with a force in the range of about +/ ⁇ 0.2 to about +/ ⁇ 0.3 g.
  • the relationship between the parts can be seen in the exploded view of the reciprocating movement platform shown in FIG. 1 .
  • the mattress 101 attaches to the mattress support 105 with Velcro strips, while the footboard frame 103 (with attached cast shoes 104 ) is bolted onto the mattress support 105 .
  • the mattress support 105 is securely attached to the drive 200 .
  • the drive 200 has four track wheels 232 located in the four top corners of the drive 200 . These wheels 232 sit in four similarly placed tracks in the box frame 800 .
  • the drive 200 , mattress support 105 , and mattress 101 form one part of the assembled movement platform, and the only physical connection between this top part and the bottom box frame 800 is the four wheels 232 of the drive 200 sitting in the four tracks of the box frame 800 .
  • the track 810 on top of the box frame 800 has rounded ends so that the wheel 232 of the drive 200 may only move a certain distance in either direction.
  • the track is beveled so that the track wheel 232 of the drive 200 will rest naturally in the center of the track.
  • the track is also located near the metal support struts of the box frame 800 which thus transfer the weight of the drive 200 (and the attached mattress support 105 , mattress 101 , and subject) directly down to the caster 830 in the corner below.
  • the box frame 800 weighs about 120 lbs. and serves at least the following five purposes: 1) supporting the rest of the platform (the drive 200 , mattress support 105 , mattress 101 , and subject); 2) providing a foundation that can be moved or anchored by means of the casters 830 ; 3) maintaining an adequate distance from surrounding walls by means of its bumpers 820 ; (4) carrying the system electronics; and (5) encasing the drive 200 for safety and noise reduction.
  • the box frame 800 provides ground clearance for the hoist legs.
  • the drive 200 weighs 200 lbs and is 24′′ wide.
  • the displacement modules in the drive 200 take the form of two pairs of rotating counterweights, connecting belts, pulleys, springs, and motors.
  • FIGS. 2A and 2B are drawings of a side view and a top view, respectively, of the drive 200 and its various mechanisms.
  • the two pairs of drive weights 215 A & 215 B and 225 A & 225 B are shown attached to their respective horizontal shafts 210 and 220 . These shafts are attached by means of struts to the frame of the drive 200 .
  • the four track wheels 232 can be seen in FIGS. 2A-2B .
  • the drive rotation motor 1700 which drives the drive weights and a linear displacement motor 260 which sets the phase difference between the two pairs of drive weights.
  • the drive rotation motor 1700 is a 180VDC 1 ⁇ 2 hp 0-1750 RPM motor, although only 1/10 hp is actually used.
  • the linear displacement motor 260 is a 9′′ per minute 400 lb. 110VAC linear displacer with 12′′ of travel.
  • FIGS. 3A-E The movement of counterweights 215 A and 215 B as seen from above is shown in FIGS. 3A-E .
  • the centers of gravity of both drive weights 215 A and 215 B are on the same line 401 from center drive shaft 210 .
  • drive weights 215 A and 215 B continue their rotations in opposite directions: drive weight 215 A in a clockwise direction, drive weight 215 B in a counter-clockwise direction.
  • FIG. 3C the drive weights have moved into positions opposite each other. This is beneficial because the force of the two drive weights are also in opposite directions and thus, negate each other's effect.
  • the rotation continues in FIG.
  • FIGS. 3A-E show how the motion of the drive weights moves the drive 200 up and down the box frame tracks (i.e., headwards and footwards for a subject on the mattress 101 ), but not sideways within the box frame 800 . If FIG. 3A is the position which causes the headward movement, FIG. 3C is the position which negates any movement, and FIG. 3E causes the footward movement.
  • the drive weights are of unequal size. This is because the weights are located at different distances from the center of drive shaft 210 . If the drive weights were the same mass, their effects would not be balanced and the drive 200 would rock sideways in the box frame 800 . However, if drive weight 215 B is a predetermined amount of mass less than drive weight 215 A, the effect of the drive weights when rotating in opposite directions will cancel each other out. Because of this arrangement, the drive weights are in the same horizontal plane as shown in FIG. 2 , which greatly reduces any shimmy effect that was produced in previous platform versions which had their drive weights in different horizontal planes. The outer edge of drive weight 215 A is 12′′ from drive shaft 210 and this outer edge travels past the very outside edge of the drive itself when rotating.
  • FIG. 2B shows the pulley system with drive belt 370 and the phase control belt 380 .
  • the drive belt 370 runs from drive rotation motor 1700 to drive shaft 210 and provides the power to rotate drive weights 215 A and 215 B around drive shaft 210 and indirectly provides the power to rotate drive weights 225 A and 225 B around shaft 220 .
  • Drive belt 370 is a 3 ⁇ 4′′ L pitch timing belt, although a timing belt is not required in this position. Because of the size of the wheel around drive shaft 210 which is driven by drive belt 370 in comparison to the size of rotation shaft, there is a 5:1 speed reduction from the drive rotation motor 1700 to the actual rotational speed of the drive weights.
  • Phase control belt 380 runs around four pulley wheels of equal size: a release pulley wheel, a drive shaft pulley wheel, secondary shaft pulley wheel, and a linear displacement pulley wheel. Because it is also attached to drive shaft 210 , the drive pulley wheel drives the phase control belt. Secondary shaft pulley wheel receives the power to rotate the drive weights around shaft 220 from the drive shaft pulley wheel through phase control belt 380 .
  • the release pulley wheel provides required tension for phase control belt 380 , and can also be used to release the tension on phase control belt 380 in order that phase control belt 380 can be taken off for repair or transport.
  • Linear displacement pulley wheel can be moved in position up and down linear shaft under the control of linear displacement motor 260 . It is by this means that the relative phases of the two pairs of drive weights are controlled.
  • the drive weights around each shaft make the same movements as shown in FIGS. 3A-3E .
  • one pair of drive weights can be moved in and out of phase with the other pair of drive weights.
  • the two pairs of drive weights are in phase when they are in the same rotational positions at the same time. Both pairs would look like FIG. 3A at the same time, like FIG. 3B at the same time, etc.
  • the two pairs are out of phase when they are not in the same rotational positions at the same time.
  • drive weights 215 A & 215 B might be in the position shown in FIG. 3A
  • drive weights 225 A & 225 B might be in the positions shown in FIG. 3B . In that case, they would be 45° out of phase with each other.
  • the relative phases of the pairs of drive weights are controlled by the linear displacement motor 360 , which controls the pulley system.
  • the speed of rotation of the pairs of drive weights are controlled by increasing or decreasing the speed of the drive rotation motor 1700 .
  • control electronics of the present invention merely control these two variables in order to get the desired effect on the subject (as described, for example, in the '962 patent, the '454 publication, and the '957 application).
  • a handheld controller with a communication link to the control electronics of the drive 200 may be used by the health care provider or the subject him- or herself, Readings of the speed and peak acceleration could also be available.
  • the control electronics also incorporate a “patient stop switch” which may be given to the subject to hold. The motors would stop whenever the switch was activated.
  • this reciprocating movement platform is well designed for providing a wide range of controlled motions to a subject on it, it is fairly heavy, and, as such, may not be appropriate for usage in the more. Thus, there is a need for a reciprocating movement platform with reduced weight.
  • the presently preferred embodiment of an apparatus of the present invention comprises a box frame, a drive module, and a support connected to the drive module.
  • the support has a planar surface for supporting the subject, and a footboard to hold the subject's feet.
  • the drive module provides periodic acceleration to the subject by moving in a line parallel to the planar surface of the support.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include the treatment and prevention of cancer as well as diminishing the unwanted side effects of chemotherapy and radiotherapy, and the chronic preconditioning, immediate preconditioning, and/or postconditioning of subjects, such as athletes, to prevent and/or treat prevent/treat any of the Examlubrious conditions which may be caused by athletic activity, whether such activity is continuous, periodic, or intermittent as well as to improve sports performance.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention also include chronic treatments to minimize organ damage caused by an unforeseen future stroke, coronary artery thrombosis, pulmonary embolism, etc.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include attenuation of left ventricular remodeling and promotion of reverse left ventricular remodeling.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include attenuation of the inflammatory and cognitive deficit complications of coronary artery bypass surgery, diminution of cardiac allograph vasculopathy as well as aiding angiogenesis in ischemic tissue.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include the cognitive and learning deficits as well as behavioral abnormalities in early cognitive impairment, Alzheimer's disease, vascular dementias, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's chorea, Wilson's disease, suprabulbar palsy and possibly Tourette syndrome.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes hereditary hemorrhagic telangiectasia.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include migraine and prion diseases.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes the ageing process and management of Sjogren's syndrome, Lyme disease, and the Gulf War syndrome.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes treatment of cystic fibrosis, chronic bronchitis, asthma, chronic sinusitis and adult and infant respiratory distress syndrome, SARS and chronic otitis media as well as the adverse effects of mechanical ventilation that cause damage to the lung.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes corticosteroid resistant asthma, Crohn's disease and ulcerative colitis.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention include improving nail growth and nail brittleness.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes preventing and treating the serious side effects of cell free hemoglobin transfusions.
  • the presently preferred medical treatments possible with externally applied periodic acceleration according to the present invention includes treatment of the consequences of injuries from a nuclear explosion, “dirty bomb” or nuclear power plant attack.
  • FIG. 1 is an exploded view of the components in a reciprocating movement platform according to embodiments of the present invention
  • FIG. 2A is a schematic drawing of a side view of a drive according to a previously described preferred embodiment of the present invention
  • FIG. 2B is a schematic drawing of a top view of a drive according to a previously described preferred embodiment of the present invention.
  • FIGS. 3A-3E are diagrams showing the movement of a single pair of drive weights according to a previously described embodiment of the present invention.
  • FIGS. 4 , 5 , and 6 are different views of a completely assembled reciprocating movement platform according to a previously described preferred embodiment of the present invention.
  • FIG. 7 shows cast shoes and a footboard support according to a previously described preferred embodiment of the present invention.
  • the present invention relates to both an apparatus and methods of treatment using periodic acceleration. This portion of the application is broken into two sections: section I will describe some preferred embodiments of the apparatus, and section II will describe methods of treatment.
  • settings of approximately ⁇ 0.20 g and rate of 140 cycles per minute and for obese adults settings of approximately ⁇ 0.17 and rate of 140 cycles per minute provide a proper balance between nitric oxide release and subject comfort during periodic acceleration treatments.
  • the amount of displacement of drive module 200 is fixed, rather than variable, as it is in the '957 application.
  • the complex machinery in the embodiments of the '957 application are no longer necessary. Specifically, there is no need for the two large, heavy electrical motors, or the complex system of fly wheel belt assemblies which provide both the speed and displacement adjustments in the '957 application.
  • the new “home unit” motion platform will provide variable speed, but fixed displacement. It will use the existing welded box frame 800 , or a bolted, wrought aluminum modular box frame (with greatly reduced weight), such as the modular elements made by Item, Solingen, Germany.
  • a simplified motor driving system will be attached to the box frame 800 rather than being contained within drive module 200 , as it is in the '957 application. This simplified motor driving system will ‘push’ and ‘pull’ drive 200 through a sinusoidal horizontal, head to foot motion of approximately 2.5 cm or less. The stroke distance is fixed during manufacture for the desired periodic acceleration gravitational setting. The cycling speed is adjusted to a given range of speeds.
  • the presently preferred drive for the home model device is a rotary eccentric mounted to box frame 800 , but coupled to drive 200 . It is powered by an adjustable AC drive motor, powered via a 120 VAC, single-phase input (50 or 60 Hz).
  • the adjustable AC drive motor provides an adjustable frequency and voltage output of 0-60 Hz, 0-230 VAC, 3-phase power.
  • An example of such a variable speed AC drive motor rated at 1 ⁇ 2 HP is manufactured by AC Tech (Model SM005S, AC Technology, Usbridge, Mass. 01569). It has an adjustable acceleration/deceleration control; the variable speed can be controlled thereby via a front panel.
  • the adjustable AC drive motor powers a three-phase induction, brushless motor from 0 to 1800 rpm with a totally enclosed, non-ventilated, flange (AG induction motor, 56C flange, TENV construction, 230VAC, 3 ph, 60 Hz, Baldor Electric Company, Fort Smith Ark. 72901) mounted to an industrial rated right angle worm reducer of 10:1 reduction that converts the rotary motion of the shaft of the AC motor into linear displacement.
  • the worm reducer is provided with an output shaft, whereupon the rotary eccentric drive is fixed and keyed.
  • the worm reducer with 56C face input is scaled for lift lubrication (Model NMRV-040-10:1-56 C, Motovario, Alpharetta, Ga. 30005).
  • a plate On the end of the worm reducer output shaft is a plate that can be securely bolted to another plate attached to the flat surface of one end of the frame of drive module 200 , thereby imparting a head to foot linear sinusoidal motion. It should be recognized that other models of the components of the drive and frame and manufacturers could be substituted for these “off the shelf” parts in the fabrication of the home periodic acceleration, motion platform device. Furthermore, different constructions and architectures may be used, as would be known to one skilled in the art, for having a motor attached to box frame 800 which imparts the head to foot motion of drive module 200 .
  • Treatments with periodic acceleration are self-limited for acute soft tissue and bone injuries. They serve as a jump-start for patients in whom aerobic exercise is one of the recommended first line treatments such as coronary artery disease, peripheral vascular disease, fibromyalgia and chronic fatigue syndrome.
  • treatment is lifetime for most chronic inflammatory diseases that encompass 1) neurological diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, neuropathy, etc., 2) rheumatological diseases such as osteoarthritis, rheumatoid arthritis, etc., 3) gastrointestinal diseases such as Crohn's disease, ulcerative colitis, etc., 4) liver diseases such as hepatitis C and portal cirrhosis, 5) kidney diseases such as glomerulonephritis, etc. 6) urinary tract diseases such as interstitial cystitis, etc. Therefore, a cheaper, simplified, periodic acceleration device of less weight than the current design is needed for home applications.
  • the external appearance may take several forms depending upon use and consumer preferences, viz., a stand alone medical device, to also serve as a single or queen size bed for sleeping, or to be incorporated into a sofa design and also serve for sitting.
  • the dimensions of the frame can be increased in width to accommodate two individuals or side-to-side periodic acceleration.
  • the use of the digital pulse wave and R wave trigger recording from the electrocardiograph during varied settings of periodic acceleration amplitude and rate in cycles per minute allows analysis of the descent of the dicrotic notch as described in the '957 application.
  • the magnitude of descent of the dicrotic notch and/or the cycle length and magnitude of the rise and fall of the dicrotic notch during periodic acceleration provides an estimate of the effectiveness of nitric oxide released from activation of endothelial nitric oxide synthase by pulsatile shear stress. This enables transfer of optimal settings from the current device to the home device that allows control of rate with a fixed setting for amplitude adjusted in the factory where the home device is manufactured.
  • Tumors in which nuclear factor kappa beta is present in the nucleus of cells include the following among others (Garg A, Agawam B. Nuclear transcription factor - kappa B as a target for cancer drug development . Leukemia 2002; 16:1053-68); Bus-Ramos C E, Roche F C, Shishodia S, Medeiros L J, Kantarjian H M, Vadhan-Raj S, Estrov Z, Smith T L, Nguyen M H Aggarwal B B. Expression of constitutively active nuclear - kappa B RelA transcription factor in blasts of acute myeloid leukemia . Hum Pathol 2004; 35: 246-253):
  • Tumorigenesis is characterized by self-sufficiency in growth signals, insensitivity to growth inhibition, evasion of apoptosis, immortalization, sustained angiogenesis, tissue invasion and metastasis.
  • Nuclear factor kappa beta that is constitutively activated in tumor cells promotes tumorigenesis since this gene produces negative feedback of nuclear factor kappa beta, causes cancer cell proliferation, prevents apoptosis (programmed cell death), increases angiogenesis, and increases metastatic potential.
  • Garg A Aggarwal B B. Nuclear transcription factor - kappa B as a target for cancer drug development .
  • vascular endothelial growth factor vascular endothelial growth factor
  • IL-8 interleukin 8
  • iNOS inducible nitric oxide synthase
  • COX2 vascular endothelial growth factor
  • VEGF vascular endothelial growth factor
  • IL-8 interleukin 8
  • COX2 vascular endothelial growth factor
  • VEGF induces proliferation of endothelial cells, increases vascular permeability, and induces activation of plasminogen activators by such cells, VEGF and IL-8 are directly expressed by tumor cells and also stimulated by nuclear factor kappa beta activation.
  • Xiong H Q Abbruzzese J L, Lin E et al. NF - kappaB activity blockade impairs the angiogenic potential of human pancreatic cancer cells .
  • Huang S Robinson J B, Deguzman A et al.
  • Blockade of nuclear factor - kappaB signaling inhibits angiogenesis and tumorigenicity of human ovarian cancer cells by suppressing expression of vascular endothelial growth factor and interleukin 8. Cancer Res 2000; 60(19):5334-5339).
  • Nitric oxide produced from iNOS in at a low level in ulcerative colitis and sporadic colorectal cancer activates p53, which is anti-tumorigenic, but at a high level of production, NO may cause mutations in p53 thereby acting in a pro-tumorigenic role.
  • the tumor suppressor p53 is a sensor of diverse cellular stresses including DNA damage, oxidative stress, and hypoxia, and aids in directing cell cycle arrest and apoptosis (physiological programmed death of cells) through transcriptional activation of target genes like p21.
  • p53 is the most commonly mutated gene in a broad spectrum of cancers and is often associated with tumor progression, resistance to therapy, and poor prognosis. In melanoma, p53 rarely mutates but increased expression associated with tumor progression correlates well with iNOS activity. Increased nitric oxide from activation of iNOS in melanoma cells also correlates with resistance to chemotherapeutic agents. (Goodman J E, Hofseth L J, Hussain S P et al. Nitric oxide and p 53 in cancer - prone chronic inflammation and oxyradical overload disease . Environ Mol Mutagen 2004; 44(1):3-9; Tang C H, Grimm E A.
  • Epidermal growth factor receptor (EGFR) is overexpressed in tumors such as lung, colon, kidney, prostate, breast, and head and neck carcinomas, which are mostly resistant to current chemotherapies. EGF prevents apoptosis or programmed death of cancer cells like nuclear factor kappa beta, thereby rendering them immortal. Activation of the EGFR-TK enzyme also results in autophosphorylation, which drives signal transduction pathways leading to tumor growth and malignant progression. When EGFR activation is blocked with anti EGFR drugs, VGFR and IL-8 production falls. However, use of anti-EGFR agents may be associated with the side effects of skin rash and diarrhea and less frequently interstitial pneumonitis.
  • the EGFR-TK inhibitor gefitinib shows clinical benefits in patients with advanced non-small cell lung cancer whose disease had previously progressed on platinum- and docetaxel-based chemotherapy regimens.
  • Lohovic G Targeting epidermal growth factor receptor signaling: early results and future trends in oncology .
  • Vlahovic G Crawford J. Activation of tyrosine kinases in cancer .
  • TNF tumor necrosis factor
  • NF-kappaB nuclear factor-kappaB
  • mitogen-activated protein kinases e.g. c-jun N-terminal kinase
  • TNF alpha is a tumor promoter and helps to produce the toxic effects associated with conventional cancer therapy, such as the cytokine release syndrome and cisplatin-induced nephrotoxicity.
  • Cyclooxygenase 2 (COX2) overexpression that is found most commonly in lung and colorectal cancers contributes to the tumorigenesis by at least five different mechanisms including transformation of procarcinogens on carcinogens, pro-inflammatory and immunomodulatory effect, resistance to apoptosis, angiogenesis and invasion progression. Therefore, treatment with a COX2 inhibitor in such tumors retards tumor progression.
  • COX2 inhibitor in such tumors retards tumor progression.
  • Adhesion of circulating tumor cells to microvascular endothelium plays an important role in tumor metastasis. Tumor cells are more likely to adhere to postcapillary venules than to corresponding precapillary arterioles thereby playing an important role in tumor metastasis to distant organs. (Kong L, Dunn G D, Keefer L K et al. Nitric oxide reduces tumor cell adhesion to isolated rat postcapillary venules . Clin Exp Metastasis 1996; 14(4):335-3).
  • Nitric oxide released from eNOS with periodic acceleration offers a non-toxic means to suppress activated nuclear factor kappa beta (Stefano G B, Prevot V, Cadet P, Dardik I. Vascular pulsations stimulating nitric oxide release during cyclic exercise may benefit health: a molecular approach ( review ), Int. J. Mol. Med. 2001; 7:119-29). Further, since tumors are characterized by a well-developed blood supply, distribution of the nitric oxide suppressant activity on activated nuclear factor kappa beta does not pose a problem.
  • Periodic acceleration through nitric oxide release from activation of eNOS suppresses activity of nuclear factor kappa beta. This was recently demonstrated in a sheep model of asthma, which is an example of an nuclear factor kappa beta disease.
  • Periodic acceleration (pGz) stimulates NO release from endothelial nitric oxide synthase (eNOS) through pulsatile shear stress (Adams et al. Effects of periodic body acceleration on the in vivo vasoactive response to N - w - nitro - L - arginine and the in vitro nitric oxide production . Ann. Biomed. Engineer. 2003;31:1337).
  • NF-kB is a transcription factor for inflammatory cytokines involved in the LAR.
  • Periodic acceleration modifies antigen - induced airway responses in sheep by nitric oxide ( NO )- mediated down regulation of nuclear factor kappa beta ( NF - kB ). Eur. Resp. J. 2004; 24: in press).
  • Nitric oxide released from eNOS with periodic acceleration acts on other tumorigenic mediators directly or indirectly through nuclear factor kappa beta.
  • Nuclear factor kappa beta regulates the expression of vascular endothelial growth factor (VEGF) and IL-8,
  • VEGF vascular endothelial growth factor
  • the decreased expression of VEGF and interleukin 8 directly correlate with decreased tumorigenicity, decreased vascularization of lesions, decreased formation of malignant ascites, and prolonged survival in several cancers, e.g., pancreatic, ovarian, etc.
  • Xiong H Q Abbruzzese J L, Lin E et al. NF - kappaB activity blockade impairs the angiogenic potential of human pancreatic cancer cells .
  • the VEGF-mediated angiogenesis requires NO production from activated endothelial NO synthase (eNOS). Activation of eNOS by VEGF involves several pathways including Akt/PKB, Ca(2+)/calmodulin, and protein kinase C.
  • eNOS activated endothelial NO synthase
  • Akt/PKB Akt/PKB
  • Ca(2+)/calmodulin Ca(2+)/calmodulin
  • protein kinase C protein kinase C.
  • the NO-mediated VEGF expression can be regulated by HIF-1 and heme oxygenase 1 (HO-1) activity, and the VEGF-mediated NO production by eNOS can be also modulated by HIF-1 and HO-1 activity, depending upon the amount of produced NO.
  • VEGF In metastatic cancers, plasma VEGF greatly exceeds normal values of VEGF, for example with metastatic lung cancers, it may be 10 times the normal value.
  • the periodic acceleration VEGF suppressant effect through inhibition of nuclear factor kappa beta activity is of greater importance in anti-tumorigenesis than the pro-tumorigenesis effect of VEGF in angiogenesis.
  • Periodic acceleration by releasing small quantities of NO from eNOS suppresses iNOS activity, which is usually pro-tumorigenic. It also scavenges reactive oxygen species (ROS) and reactive nitrogen species (RNS) that are pro-tumorigenic (Stefano G B, Goumon Y, Bilfinger T V et al. Basal nitric oxide limits immune, nervous and cardiovascular excitation: human endothelia express a mu opiate receptor . Prog Neurobiol 2000; 60(6):513-530). This action of periodic acceleration therefore may help to prevent and treat colorectal and other cancers. (Hussain S P, Amstad P, Raja K et al.
  • the tumor suppressor p53 is a sensor of diverse cellular stresses including DNA damage, oxidative stress, and hypoxia, and helps to direct cell cycle arrest and apoptosis through transcriptional activation of target genes like p21.
  • p53 is the most commonly mutated gene in a broad spectrum of cancers and is frequently associated with tumor progression, resistance to therapy, and poor prognosis. In melanoma, p53 rarely mutates but increased expression associated with tumor progression and correlates well with iNOS activity.
  • Nitric oxide from NO donor drugs transiently and reversibly inhibits epidermal growth factor receptors (EGFR) in neuroblastoma cells.
  • EGFR epidermal growth factor receptor
  • Activation of the EGFR-TK enzyme results in autophosphorylation, which drives signal transduction pathways leading to tumor growth and malignant progression.
  • EGF prevents apoptosis of cancer cells prevents apoptosis thereby immortalizing tumor cells.
  • VGFR and IL-8 production also contribute to tumor regression.
  • Nitric oxide from eNOS activation with periodic acceleration suppresses tumor necrosis factor superfamily indirectly through inhibition of nuclear factor kappa beta.
  • Periodic acceleration through shear stress suppresses tumor necrosis factor alpha activity independently of activation of eNOS.
  • NO from eNOS reduces tumor cell adhesion to blood vessels and also suppresses adhesion molecules thereby suppressing tumor metastases.
  • Nitric oxide reduces tumor cell adhesion to isolated rat postcapillary venules . Clin Exp Metastasis 1996; 14(4):335-343; Stefano G B, Goumon Y, Bilfinger T V et al. Basal nitric oxide limits immune, nervous and cardiovascular excitation: human endothelia express a mu opiate receptor . Prog Neurobiol 2000; 60(6):513-530.
  • nitric oxide released by activation of eNOS with periodic acceleration may be improved by vitamin and dietary supplements thereby enhancing its effects in cancer treatment as well as treatment of any condition that requires increased levels of nitric oxide from eNOS. This may be of importance where endothelial function is compromised such as in arteriosclerosis.
  • L-ascorbic acid vitamin C
  • Vitamin C also increases tetrahydrobiopterin and NOS activity in blood vessels.
  • vitamin C The beneficial effect of vitamin C on vascular endothelial function appears to be mediated in part by protection of tetrahydrobiopterin and restoration of eNOS enzymatic activity. Prolonged high activity of iNOS may be detrimental to vascular function due to “uncoupling” of eNOS and subsequent formation of reactive oxygen species (ROS).
  • ROS reactive oxygen species
  • endothelial nitric oxide (NO) synthase eNOS
  • eNOS endothelial nitric oxide synthase
  • BH4 tetrahydrobiopterin
  • Tetrahydrobiopterin restores endothelial dysfunction induced by an oral glucose challenge in healthy subjects .
  • folic acid administration exerts direct anti-oxidative effects and contributes to restoration of impaired NO metabolism.
  • Folate also reduces plasma homocysteine levels, enhances eNOS, and has anti-inflammatory actions. It stimulates endogenous BH4 regeneration, a cofactor necessary for NO synthesis from eNOS, inhibits intracellular superoxide generation, and thus enhances the half-life of NO. BH4 in turn enhances NO generation and augments arginine transport into the cells.
  • Folic acid increases the concentration of omega-3 PUFAs, which also upregulates eNOS synthesis.
  • Vitamin C augments NO synthesis from eNOS by increasing intracellular BH4 and stabilization of BH4.
  • Suder O Weger M. Interactions of homocysteine, nitric oxide, folate and radicals in the progressively damaged endothelium . Clin Chem Lab Med 2003; 41(11):1444-1454; Das U N. Folic acid says NO to vascular diseases. Nutrition 2003; 19(7-8):686-692.).
  • there appears to be a benefit of higher folic acid consumption in reducing risks of colon and breast cancers. (Willett W C. Diet and cancer .
  • the dose of niacin (Niaspan, KOS) is initiated at 375 mg at night and titrated to a maximal tolerated dose of 1500 mg. Patients take aspirin 30 minutes prior to niacin to minimize side effects.
  • KOS niacin
  • Such a supplement plan may be used in conjunction with periodic acceleration to enhance its effects on eNOS.
  • Das′ recommendation for the dose of L-Arginine is probably an underestimate.
  • Oral supplementation with large amounts (6-21 g/day) of L-arginine, the precursor of endothelial-derived nitric oxide improves endothelium-mediated vasodilation in hypercholesterolemia.
  • Flow mediated vasodilation is improved with 6.6 g of L-Arginine administered for in the form of a nutrient bar.
  • Maxwell A J, Anderson B, Zapien M P et al. Endothelial dysfunction in hypercholesterolemia is reversed by a nutritional product designed to enhance nitric oxide activity .
  • Cardiovasc Drugs Ther 2000; 14(3):309-316. Lower doses are ineffective.
  • High dosage niacin may be administered in the presence of endothelial dysfunction to produce further upregulation of eNOS.
  • Both the immediate and late complications of radiation and/or chemotherapy may be ameliorated by periodic acceleration as pre-treatment, during treatment and post-treatment. Because radiation-induced vascular injury precedes the tissue damage, vascular injury is regarded as crucial in the pathogenesis of tissue damage. Radiation injury is marked by activation of adhesion molecules that promote leukocyte infiltration of normal tissue. Radiation activates nuclear factor kappa beta, which in turn activates adhesion molecules. (Quarmby, S.; Kumar, P.; Kumar, S. Radiation - induced normal tissue injury: role of adhesion molecules in leukocyte - endothelial cell interactions . Int. J. Cancer 1999;82 — 385-395.) Radiotherapy and chemotherapy produce numerous adverse early and late complications.
  • GI mucositis a frequent complication of anticancer treatment, threatens the effectiveness of therapy because it leads to dose reductions, increases healthcare costs, and impairs patients' quality of life.
  • periodic acceleration alone or in conjunction with chemotherapeutic or x-ray or other cancer suppressing agents or technology offers a way to treat cancers. It may permit lesser doses of radiation and/or chemotherapy thereby minimizing deleterious side effects. Furthermore, application of periodic acceleration either alone or with other preventative agents can be used to prevent cancers. Treatment with periodic acceleration avoids the late effects of radiotherapy and chemotherapy on normal tissues. The late onset of necrosis and fibrosis in normal tissues can be a serious consequence of radiotherapy and chemotherapy in cancer patients. Because radiation-induced vascular injury precedes the tissue damage, vascular injury is regarded as crucial in the pathogenesis of tissue damage. Radiation injury is marked by activation of adhesion molecules that promote leukocyte infiltration of normal tissue.
  • chest or mantle radiotherapy breast cancer, thyroid cancer, hypothyroidism, pulmonary fibrosis, lung cancer, cardiac fibrosis, pericarditis, etc
  • abdominal/pelvic radiotherapy chronic enteritis, gastrointestinal malignancy, renal failure, hemorrhagic cystitis, bladder cancer, ovarian failure, testicular failure, etc.
  • any radiation skin cancer, melanoma, sarcoma, etc.
  • Late effects of chemotherapy depend upon the drug and may cause the following: 1) alkylating agents (e.g., cyclophosphamide, chlorambucil, bisulfan, procarbazine, etc.)—hypogonadism, early menopause, acute myeloid leukemia, pulmonary fibrosis, bladder fibrosis, renal failure, etc., 2) cisplatin/carboplatin—hearing loss, vertigo, tinnitis, renal failure, etc., 3) methotrexate—neurocognitive deficits, 4) anthracyclines (e.g., doxorubacin, daunorubicin, etc.)—cardiomyopathy, arrhythmia, and 4) bleomycin—interstitial pneumonitis, pulmonary fibrosis, 5) corticosteroids—osteopenia, osteoporosis, avascular necrosis, 6) epepodophylloxins—acute mye
  • periodic acceleration has a place in management of cancer either as a stand-alone modality or complimentary to radiotherapy and chemotherapy regimens.
  • Periodic acceleration evokes widespread release of nitric oxide throughout body—wherever there is a blood vessel, pulsatile shear stress promotes expression of nitric oxide that suppresses directly or indirectly pro-tumorigenic mediators.
  • nitric oxide that suppresses directly or indirectly pro-tumorigenic mediators.
  • pro-tumorigenic mediators include nuclear factor kappa beta, vascular endothelial growth factor, inteleukin-8, epidermal growth factor receptor, tumor necrosis superfamily, inducible nitric oxide synthase, mutated p53, COX2, and adhesion molecules.
  • Periodic acceleration does not harm healthy cells nor produce deleterious side effects in contrast to radiotherapy and chemotherapy thereby avoiding the late fibrotic effects of radiation and chemotherapy on normal tissues. Periodic acceleration cannot cause overdose of endothelial-derived mediators. Periodic acceleration is complementary to conventional cancer therapies without adverse “drug” interactions.” Periodic acceleration is synergistic or additive in suppression of tumorigenesis to radiotherapy and chemotherapy. Periodic acceleration mitigates the early and late complications of radiotherapy and chemotherapy. Periodic acceleration may be utilized chronically as a cancer prevention measure. Vitamin supplements, antioxidants, and phytochemicals in conjunction with periodic acceleration may increase the effectiveness of NO release from eNOS, with potential for greater suppression of nuclear factor kappa beta and other inflammatory mediators in tumors.
  • NSAIDs non-steroidal anti-inflammatory drugs
  • sprains and contusions suggest that their use can result in a modest inhibition of the initial inflammatory response and its symptoms. This may be associated with slight negative effects later in the healing phase.
  • Corticosteroids have generally been shown to adversely affect the healing of these acute injuries.
  • the beneficial effect of NSAIDs on improvement of delayed-onset of muscle soreness appears to be minimal.
  • nitric oxide released from eNOS suppress strenuous exercise induced activation of nuclear factor kappa beta thereby diminishing IL-1beta, IL-6, tumor necrosis factor and other inflammatory cytokines and adhesion molecules.
  • small quantities of nitric oxide from eNOS suppress activity of iNOS (Stefano G B, Prevot V, Cadet P, Dardik I. Vascular pulsations stimulating nitric oxide release during cyclic exercise may benefit health: a molecular approach ( review ). Int. J. Mol. Med. 2001; 7:119-29). This is important because large amounts of nitric oxide are released after strenuous exercise in professional football players and other athletes that are associated with severe muscle cramps.
  • periodic acceleration can mitigate skeletal muscular cramps during an athletic event, and help to prevent muscle strains during an event as well as delayed onset muscular soreness (DOMS) and involuntary muscle cramps and spasms immediately following the athletic event and delayed until the sleeping hours. It has been found that an additional periodic acceleration treatment administered four to eight hours after the athletic event provides even better relief than a single pretreatment in relieving nocturnal muscle cramps.
  • DOMS delayed onset muscular soreness
  • Cardiac troponin T (cTnT) and troponin I (cTnI) are highly sensitive and specific for detecting myocardial damage even in the presence of skeletal muscle injury.
  • Ultraendurance exercise may cause myocardial damage as indicated by elevations of these biochemical cardiac-specific markers and also by echocardiography (Rifai N, Douglas P S, O'Toole M, Rimm E, Ginsburg G S. Cardiac troponin T and I, echocardiographic [correction of electrocardiographic] wall motion analyses, and ejection fractions in athletes participating in the Hawaii Ironman Triathlon , Am. J. Cardiol.
  • eNOS Activation of eNOS to release small quantities of nitric oxide preconditions the heart against the adverse effects of compromise of the blood supply to the heart that produces myocardial damage.
  • Periodic acceleration activates eNOS through increased pulsatile shear stress and, as such, is a means to precondition the heart.
  • Endogenous nitric oxide 1) reduces myocardial oxygen consumption and thus improves regional myocardial function for any given level of myocardial blood flow, oxygen consumption and energetics, 2) preserves contractile calcium sensitivity during myocardial ischemia, and 3) contributes to hibernation, i.e., adaptation to myocardial ischemia, by preserving regional contractile function without any effect on myocardial energetics (Heusch G, Post H, Michel M C, Kelm M, Schulz R. Endogenous nitric oxide and myocardial adaptation to ischemia . Circ. Res. 2000; 87:146-52). Since the limitation to athletic activities often is the amount of blood pumped by the heart through the body, preconditioning with periodic acceleration serves to optimize athletic performance.
  • Exercise-induced bronchospasm i.e., an asthmatic episode
  • EIB Exercise-induced bronchospasm
  • This factor limits athletic capabilities.
  • nitric oxide is generated from the athlete's own body.
  • periodic acceleration treatments administered prior to an athletic event minimize delayed onset of muscle soreness (DOMS) and nocturnal muscle spasms.
  • An additional periodic acceleration treatment administered four to eight hours following cessation of the athletic event provides even further relief.
  • Periodic acceleration administered prior to strenuous athletic events minimizes microscopic myocardial damage.
  • Chronic treatment with periodic acceleration improves sports performance by promoting mitochondrial biogenesis.
  • Periodic acceleration administered prior to an athletic event protects against exercise induced asthma. Since many athletic venues do not permit effective drugs for the treatment of asthma because of they also improve performance unrelated to alleviation of asthma, pretreatment of competitive athletes can be accomplished with periodic acceleration to prevent exercise induced asthma.
  • Chronic periodic acceleration treatments should minimize damage that might occur with ischemic events such as stroke, coronary thrombosis, pulmonary embolism, etc.
  • nitric oxide deficient mice eNOS knockout mice were significantly heavier than normal wild-type mice over the entire observation period even though dietary intake and activity were controlled and the same.
  • the NO deficient had lesser oxygen consumptions and fewer mitochondria in brown adipocytes than the wild type mice.
  • the investigators concluded that eNOS regulates mitochondrial biogenesis, energy expenditure and heat production. They noted that NOS deficiency reduced energy expenditure and produced weight gain, insulin resistance, and hypertension, which are typical features of the metabolic syndrome. (Nisoli E, Clementi E, Paolucci C et al. Mitochondrial biogenesis in mammals: the role of endogenous nitric oxide .
  • Cachexia which is marked by severe weight loss, is the opposite of obesity yet it too may respond to upregulation of eNOS but by a totally different mechanism.
  • weight loss mostly due to skeletal muscle atrophy, is a frequent and clinically relevant problem in patients with chronic obstructive pulmonary disease (COPD) as well as in patients with neoplasms.
  • COPD chronic obstructive pulmonary disease
  • activation of nuclear factor kappa beta and iNOS induction takes place in the skeletal muscle and contributes to the molecular pathogenesis of cachexia along with other inflammatory cytokines.
  • Thorax 2004; 59(6):483-487) Periodic acceleration by increasing release of small amounts of nitric oxide from eNOS suppresses nuclear factor kappa beta and iNOS activities thereby ameliorating the skeletal muscle pathology.
  • deficiency of eNOS causes less muscle oxidative capacity as well as the activities of energy metabolism enzymes in oxidative (soleus) muscle.
  • NOS Endothelial nitric oxide synthase
  • periodic acceleration treatments control weight, ameliorate the metabolic syndrome, improve sports performance, and improve skeletal muscle pathology associated with the cachexia of COPD and cancers.
  • Ventricular remodeling While current therapeutic strategies are designed to restore blood flow to the ischemic myocardium and limit infarct size, adverse left ventricular remodeling progressing to dysfunction remains a significant complication following myocardial infarction. Ventricular remodeling also takes place in conditions associated with volume overload. Ventricular remodeling consists of change from an elliptical to a spherical left ventricular volume with concomitant increase of end-systolic and end-diastolic diameters. Reverse remodeling means a reversal of ventricular shape toward a normal shape. In myocardial infarctions, the extracellular matrix (ECM) is a key component in the remodeling process through increases of collagen in the infarct area that replace necrotic myocytes to form a scar.
  • ECM extracellular matrix
  • MMP matrix metalloproteinases
  • cardiac mast cells play a major role in regulating MMP activity in ventricular remodeling.
  • Brower G L Chancey A L, Thanigaraj S et al. Cause and effect relationship between myocardial mast cell number and matrix metalloproteinase activity .
  • mast cells and bradykinin in the cardiac interstitium that modulates the pattern of LV remodeling in the acute phase of volume overload.
  • Wei C C, Lucchesi P A Tallaj J et al. Cardiac interstitial bradykinin and mast cells modulate pattern of LV remodeling in volume overload in rats .
  • Cardiac mast cells and chymase are important modulators of MMP activity and extracellular matrix degradation that contribute to adverse left ventricular remodeling in chronic volume overload secondary to mitral regurgitation.
  • caspase-3 Another mediator that promotes ventricular remodeling is caspase-3 that is activated by myocardial stunning following myocardial ischemia.
  • caspase-3 promotes cleavage of troponin-I, an important component of the cardiac contractile apparatus, and death or apoptosis of cardiomyocytes. Inhibition of caspase-3 by pharmacological agents causes less cleavage of tropomin-1 and fewer apoptotic cardiomyocytes.
  • Left ventricular reverse remodeling takes place in animals after administration of drugs that increase activity of eNOS.
  • Celiprolol stimulates endothelial nitric oxide synthase expression and improves myocardial remodeling in deoxycorticosterone acetate - salt hypertensive rats . J Hypertens 2001; 19(4):795-801; Kobayashi N, Hara K, Watanabe S et al. Effect of imidapril on myocardial remodeling in L - NAME - induced hypertensive rats is associated with gene expression of NOS and ACE mRNA .
  • Periodic acceleration through release of NO from eNOS promotes left ventricular reverse remodeling because it suppresses the activity of several mediators that play in role in promoting left ventricular remodeling including tumor necrosis factor alpha and caspase-3.
  • Periodic acceleration also prevents cardiac mast cell degranulation as a result of the increased nitric oxide from eNOS.
  • heparin also prevents mast cell degranulation and activated eNOS to release NO.
  • periodic acceleration administered early in situations that promote left ventricular remodeling such as acute myocardial infarction and ventricular volume overload from mitral regurgitation, aortic regurgitation and arteriovenous fistula attenuates ventricular remodeling.
  • Administration of periodic acceleration after ventricular remodeling has developed promotes beneficial reverse ventricular remodeling.
  • drugs that stabilize cardiac mast cells such as non-coagulant and coagulant heparin and cardiac drugs that activate eNOS such as ACE inhibitors as well as heparin produce additive or synergistic effects.
  • Atrial fibrillation may occur in susceptible patients as a result of electrical remodeling of the atria due to oxidative stress or inflammation.
  • statins have been shown to prevent atrial fibrillation in patients with coronary artery disease independent of their cholesterol lowering properties.
  • Atrial fibrillation is associated with decreased expression of eNOS in left atrial tissue because of turbulent flow in the atrium.
  • Decreased NO is associated with lack of inhibition of prothrombotic protein plasminogen activator inhibitor-1 (PAI-1) and therefore predisposes to atrial thrombus formation, a serious complication that can lead to stroke.
  • PAI-1 prothrombotic protein plasminogen activator inhibitor-1
  • chronic periodic acceleration treatments is patients susceptible to atrial fibrillation because of enlarged left atrium, e.g., mitral stenosis, mitral regurgitation, chronic heart failure, can be administered prophylactically.
  • chronic periodic acceleration can prevent the formations of left atrial thrombosis.
  • Myocardial tumor necrosis factor alpha production and nuclear factor kappa B activation has been demonstrated in chronic heart failure and experimental models of acute ischemia-reperfusion injury. Further, a cause and effect relationship has been established between these events and cardiomyocyte apoptosis (cell death) following such conditions.
  • coronary artery bypass grafting results in activation of NF-kappaB and an increase of tumor necrosis factor alpha in the heart. (Meldrum D R, Partrick D A, Cleveland J C, Jr. et al. On - pump coronary artery bypass surgery activates human myocardial NF - kappaB and increases TNF - alpha in the heart .
  • LTP Long-term potentiation
  • periodic acceleration by releasing NO from eNOS plays a major role in management of complications of coronary artery bypass surgery.
  • periodic acceleration treatments administered prior to and after coronary artery bypass surgery attenuate the inflammatory effects of cardiopulmonary bypass that can lead to the systemic inflammatory response and organ failure.
  • Periodic acceleration treatments administered prior to and after coronary artery bypass surgery can mitigate the cognitive and learning deficits that are common after cardiopulmonary bypass surgery in part by improving red cell deformability with easier capillary passage.
  • Periodic acceleration treatments can attenuate the obstructive sleep apnea syndrome commonly observed in patients with coronary artery disease.
  • Treatments with periodic acceleration also improve cognitive impairments and dementia because nitric oxide released from eNOS improves cerebral blood flow and long-term potentiation (LTP), a persistent increase in synaptic strength of nerves implicated in certain forms of learning and memory as described above.
  • LTP long-term potentiation
  • This is of particular importance in management of mild cognitive impairment, defined as memory complaints with objective memory impairment, without dementia, impairment of general cognitive functioning, or disability in activities of daily living.
  • mild cognitive impairment defined as memory complaints with objective memory impairment, without dementia, impairment of general cognitive functioning, or disability in activities of daily living.
  • this was a good predictor of Alzheimer's disease with an annual conversion rate of 8.3% and good specificity, but very unstable over time: Within 2 to 3 years, only 6% of the subjects continued to have MCI, whereas >40% reverted to normal.
  • Mild cognitive impairment refers to the transitional zone between normal ageing and dementia and may be the optimum stage to intervene with preventive therapies such as periodic acceleration.
  • Cognitive dysfunction is a major component of several neurological diseases such as Alzheimer's disease and vascular dementia.
  • Alzheimer's disease is a vasocognopathy: a new term to describe its nature . Neurol Res 2004; 26(5):517-524.
  • Alzheimer's disease characteristically produces a remarkably pure impairment of memory. Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that diffusible oligomeric assemblies of the amyloid beta protein cause the synaptic dysfunction.
  • Selkoe D J. Alzheimer's disease is a synaptic failure .
  • Parkinson's disease can also exhibit cognitive and behavioral impairments. These impairments may be attributed to dysfunction of multiple systems associated with the disease process in Parkinson's disease that are not necessarily related to motor symptoms.
  • considerable attention has addressed to disruption of the circuits in patients with Parkinson's disease connecting the frontal cortical regions and the basal ganglia (i.e., frontostriatal circuits) and how they mediate cognition and behavior in humans.
  • frontostriatal circuits i.e., frontostriatal circuits
  • Frontalstrial synapses are also disrupted in other movement disorders such as Huntington's chorea and Wilson's disease in animal models, probably suprabulbar palsy and possibly Tourette syndrome.
  • Huntington's chorea and Wilson's disease in animal models, probably suprabulbar palsy and possibly Tourette syndrome.
  • Parkinsone L A et al Abnormal synaptic plasticity and impaired spatial cognition in mice transgenic for exon 1 of the human Huntington's disease mutation . J Neurosci 2000; 20(13):5115-5123; Doreulee N, Yanovsky Y, Haas H L. Suppression of long - term potentiation in hippocampal slices by copper .
  • frontalstriatal circuits appear to be disrupted or impaired in Alzheimer's disease, vascular dementia Parkinson's disease and amyotrophic lateral sclerosis, Huntington's chorea, Wilson's disease, suprabulbar palsy thereby causing memory and learning deficits association with long term depression of the synaptic pathways.
  • Long-term potentiation a persistent increase in synaptic strength is favorable for certain forms of learning and memory. It has been found that eNOS from endothelial cells, rather than nNOS, generates NO within the postsynaptic cell as a means of producing LTP. (O'Dell T J, Huang P L, Dawson T M et al.
  • Impairment of NO-synthesis in eNOS deficient mice shifts striatal plasticity from long term potentiation to long term depression. Since computation of perivascular NO gradients from the vessel wall of capillaries indicates that targets 200 um distant can still be reached by NO, this is consistent with the possibility that NO released from eNOS participates in the modulation of cortico-striatal plasticity.
  • the added pulses produced with periodic acceleration is superior to nonpulsatile blood flow.
  • Baba et al used a pump to bypass the heart that produced pulsatile and nonpulsatile flow in goats and observed bulbar conjunctiva capillaries with a digital high definition microscope.
  • the velocity of erythrocytes in many capillaries dropped and remained at a low level, and the number of perfused capillaries decreased.
  • the velocity of erythrocytes recovered to the initial level. In many cases, the flow of nonperfused capillaries recovered to the initial level as well.
  • pulsatile flow enhanced the basal and flow-stimulated endothelium-derived nitric oxide release in the microvessels.
  • periodic acceleration is indicated as prophylactic and therapeutic treatment for cognitive and learning deficits as well as behavioral abnormalities in early cognitive impairment, Alzheimer's disease, vascular dementias, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's chorea, Wilson's disease, suprabulbar palsy and possibly Tourette syndrome.
  • Accelerated graft atherosclerosis is a key feature of most chronic rejection syndromes.
  • Atherosclerosis diffusely involves the coronary circulation.
  • Cardiac allograft vasculopathy is the most aggressive form of atherosclerosis in humans and is the leading cause of death after the first year of heart transplantation.
  • Endothelial dysfunction is a major contributing factor to the acceleration of coronary vascular disease in these individuals. Alteration in endothelial function contributes to vascular inflammation and progression of the disease. (Weis M, Cooke J P. Cardiac allograft vasculopathy and dysregulation of the NO synthase pathway . Arterioscler Thromb Vasc Biol 2003; 23(4):567-575.).
  • Periodic acceleration ameliorates the endothelial dysfunction responsible for this syndrome.
  • Endothelial nitric oxide synthase is essential for neovascularization. Impaired neovascularization in mice lacking eNOS is related to a defect in progenitor cell mobilization owing to reduced vascular endothelial growth factor (VEGF)-induced mobilization of endothelial progenitor cells (EPCs).
  • VEGF vascular endothelial growth factor
  • EPCs endothelial progenitor cells
  • vascular endothelial growth factor VEGF
  • Aerobic exercise by release of NO from eNOS increases vascular endothelial growth factor (VEGF) with consequent increase of endothelial progenitor cells.
  • VEGF vascular endothelial growth factor
  • Aerobic exercise by release of NO from eNOS increases vascular endothelial growth factor (VEGF) with consequent increase of endothelial progenitor cells.
  • VEGF vascular endothelial growth factor
  • CRP C-Reactive Protein
  • Periodic acceleration like aerobic exercise promotes mobilization of endothelial progenitor cells into the circulation as well as suppression of CRP if elevated. Periodic acceleration aids in promoting angiogenesis in ischemic tissues.
  • Hereditary hemorrhagic telanglectasis is caused by a genetic deficiency of endoglin. Endoglin also regulates transforming growth factor beta 1; In turn this mediator causes under-expression of eNOS that leads to development of abnormal blood flow passages and the manifestations of the disease.
  • eNOS transforming growth factor beta 1
  • eNOS transforming growth factor beta 1
  • eNOS transforming growth factor beta 1
  • eNOS transforming growth factor beta 1
  • eNOS transforming growth factor beta 1
  • These patients experience frequent bleedings with increasing age, in particular from the nasal, gastrointestinal, and cerebral vascular beds.
  • Vascular arteriovenous malformations develop that vary in size from 1 mm to several centimeters. Pulmonary vascular arteriovenous malformations are particularly life threatening because of bleeding. or paradoxical embolism causing brain infarction or brain abscess.
  • hereditary hemorrhagic telangiectasis is mutated genes identified as endoglin and ALK-1. They mediate binding on signaling of transforming growth factor beta.
  • the disease develops as a result of deficient TGF beta signaling in vascular endothelial cells that produces abnormal blood vessel development.
  • Jerkic M Rivas-Elena J V, Prieto M et al. Endoglin regulates nitric oxide - dependent vasodilatation . FASEB J 2004; 18(3):609-611; van den D S, Mummery C L, Westermann C J.
  • Hereditary hemorrhagic telangiectasia an update on transforming growth factor beta signaling in vasculogenesis and angiogenesis . Cardiovasc Res 2003; 58(1):20-31.
  • Periodic acceleration helps in the management of hereditary hemorrhagic telangiectasia because it addresses the underlying cause of this disease, i.e., under-expression of eNOS.
  • Nitric oxide generated from inducible nitric oxide synthase participates in immune and inflammatory responses in many tissues.
  • the NO donor glyceryl trinitrate (GTN) provokes delayed migraine attacks when infused into migraineurs and also causes iNOS expression and delayed inflammation within rodent dura mater.
  • Intravenous GTN increases NO production within macrophages.
  • iNOS expression is preceded by significant nuclear factor kappa beta activity after GTN infusion. Nuclear factor kappa beta activation and iNOS expression are attenuated by parthenolide (3 mg/kg), the active constituent of feverfew, an anti-inflammatory drug used for migraine treatment.
  • GTN promotes NF-kappaB activity and inflammation with a time course consistent with migraine attacks in susceptible individuals. Therefore, blockade of NF-kappaB activity provides a target for the anti-migraine treatment.
  • NF-kappaB activity provides a target for the anti-migraine treatment.
  • Prion diseases Mad Cow and Creutzfeldt-Jakob diseases, are devastating lethal neurological diseases which currently are untreatable.
  • examination of brain tissue from these patients reveals inflammation marked by accumulation of COX-1-expressing macrophages/microglial cells and COX-2-expressing neurons, and increased nuclear factor kappa beta and iNOS activity, (Bacot S M, Lenz P, Frazier-Jessen M R et al.
  • Activation by prion peptide PrP 106-126 induces a NF - kappaB - driven proinflammatory response in human monocyte - derived dendritic cells .
  • ROS Reactive oxygen species
  • RNS reactive nitrogen species
  • Activated nuclear factor kappa beta produces oxidative stress via the induction of MnSOD and contributes the ageing process.
  • Bacnard D Gosselin K, Monte D et al. Involvement of Rel/nuclear factor - kappaB transcription factors in keratinocyte senescence . Cancer Res 2004; 64(2):472-481.
  • Chronic inflammation accounts for effects of susceptibility to infection in aged animals.
  • the increased expression of proinflammatory cytokines and inflammatory responsive genes in the lung plays a role in the increased susceptibility in aging animals to endotoxic stress.
  • Chang C K LoCicero J, III.
  • Overexpressed nuclear factor kappaB correlates with enhanced expression of interleukin -1 beta and inducible nitric oxide synthase in aged murine lungs to endotoxic stress .
  • Ann Thorac Surg 2004; 77(4):1222-1227 Since NO from eNOS increases mitochondrial number in skeletal muscle, this might reverse aging. (Brown G C. NO says YES to mitochondria . Science 2003; 299:838-839.) Therefore, periodic acceleration alone and with caloric restriction as an additive or synergistic effect might favorably modify the ageing process.
  • Sjogren's syndrome is marked by xeropthalmia (dry eyes) and xerostomia (dry mouth) due to lymphocytic infiltrates of lacrimal and salivary glands. It may occur alone or in association with several other autoimmune diseases.
  • the clinical features involve a wide variety of organs, including skin, eyes, oral cavity and salivary glands, and systems, including nervous, musculoskeletal, genitourinary and vascular.
  • the dryness symptoms can be found in a number of other disorders including rheumatoid arthritis, systemic lupus erythematosus, scieroderma, primary biliary cirrhosis, and other rheumatic disorders.
  • the Lyme disease agent Borrelia burgdorferi , a spirochete, causes infection by migration through tissues, adhesion to host cells, and evasion of immune clearance.
  • the infection is introduced by a tick bite and cause a skin rash and persistent flu-like symptoms and fever in the summer. If inadequately treated, arthritis, cardiac arrhythmia marked by heart block, facial nerve palsy, meningitis, polyneuropathy and encepalopathy may occur. (Steere A C, Coburn J, Glickstein L. The emergence of Lyme disease .
  • Lyme disease The systemic symptoms of Lyme disease are due in part to activation of nuclear factor kappa beta with intense inflammatory cytokine expression with inflammation of microglia.
  • J Immunol 1997; 158(7):3285-3292; Rasley A, Anguita J, Marriott I. Borrelia burgdorferi induces inflammatory mediator production by murine microglia.
  • the Gulf War syndrome consists of multisymptom illnesses characterized by persistent pain, fatigue, and cognitive symptoms that have been reported by many Gulf War veterans. Vaccinations against biological warfare using pertussis were utilized as an adjuvant in such patients. This could trigger neurodegeneration through induction of interleukin-1beta secretion in the brain. Particular susceptibility for IL-1beta secretion and potential distant neuronal damage could provide an explanation for the diversity of the symptoms.
  • the symptoms in many of these patients are similar to the chronic fatigue syndrome and those with severe fatiguing illness have shown plasma immunological abnormalities but not as a universal finding. No measurements have been made of inflammatory cytokines in the cerebrospinal fluid where detection of pathology would be more likely to occur.
  • Nitric oxide released from eNOS with periodic acceleration has a potent anti-inflammatory action through suppression of nuclear factor kappa beta.
  • Perodic acceleration has been utilized in the treatment of fibromyalgia and chronic fatigue syndrome, entities with symptoms similar to those in the Gulf War syndrome. The dramatic improvement in symptoms of fibromyalgia and chronic fatigue syndrome was attributed to suppression of an inflammatory process in the brain. (Sackner M A, Gummels E M, Adams J A. Say NO to fibromyalgia and chronic fatigue syndrome: an alternative and complementary therapy to aerobic exercise .
  • nitric oxide expressed from activation of eNOS
  • periodic acceleration improves mucociliary clearance, increases pulmonary surfactant productions and minimizes the volutrauma and barotrauma of positive pressure mechanical ventilation.
  • Nitric oxide improves nasal mucociliary clearance by increasing ciliary beat frequency.
  • treatment with periodic acceleration is indicated in medical conditions associated with production of excessive bronchopulmonary and nasal secretions such as cystic fibrosis, bronchial asthma, chronic bronchitis and chronic sinusitis.
  • Periodic acceleration should be helpful in shortening duration of the mucous surface.
  • constitutional symptoms are alleviated by NO suppression of nuclear factor kappa beta activity that directs inflammatory cytokine production.
  • Physiological concentration as those released from eNOS stimulate pulmonary surfactant production and therefore periodical acceleration is indicated in the management of the adult and infant respiratory distress syndrome as well as SARS.
  • Corticosteroid therapy resistance is a common indication for surgery in inflammatory bowel disease, with as many as 50% of patients with Crohn's disease and approximately 20% of patients with ulcerative colitis requiring surgery in their lifetime.
  • proinflammatory mediators including nuclear factor kappa B, resulting in inhibition of glucocorticoid receptor transcriptional activity.
  • Hemoglobin-based oxygen carriers are being developed for use in blood replacement therapies, either for perioperative hemodilution or for resuscitation from hemorrhagic blood loss. There is a high demand for these products because of risks associated with blood transfusions and pending worldwide blood shortages. The primary adverse effect for the majority of cross-linked or polymerized cell free hemoglobin products is increased vascular resistance to blood flow. (Vandegriff K D. Haemoglobin - based oxygen carriers .
  • a major threat facing the world today is the possibility of a nuclear terrorist attack through a conventional nuclear weapon or a “dirty bomb” (combination of coventional explosive and nuclear material) or through an attack on a nuclear power plant site.
  • Some deaths from an explosion would result from direct contact with the explosive and debris but the majority of early deaths would result from infections related to bone marrow suppression of neutrophils.
  • Radiation to the abdomen can produce acute enteritis characterized by diarrhea and chronic enteropathy (hemorrhage and ulceration) which leads to progressively reduced mobility.
  • Fistulas, strictures and malabsorption are potentially life threatening.
  • Tumor necrosis factor alpha and IL-6 contribute significantly to leukemias and radiation pneumonitis.
  • vascular injury is regarded as crucial in the pathogenesis of tissue damage.
  • Radiation injury is marked by activation of adhesion molecules that promote leukocyte infiltration of normal tissue.
  • the stress of radiation activated nuclear factor kappa beta in turn promotes activation of adhesion molecules.
  • the inflammatory mediators activated in radiation injury are regulated by nuclear factor kappa beta, the key gene directing the inflammatory response. (Linard C, Marquette C, Mathieu J et al. Acute induction of inflammatory cytokine expression after gamma - irradiation in the rat: effect of an NF - kappaB inhibitor .

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US20080306563A1 (en) * 2007-06-05 2008-12-11 Jose Roberto Kullok System and method for cardiovascular treatment or training
US8266743B2 (en) 2010-08-23 2012-09-18 Midmark Corporation Examination table with motion tracking
WO2014055348A1 (en) * 2012-10-04 2014-04-10 Ventaerx, Inc. Methods and apparatuses for increasing mucociliary clearance
US8764789B2 (en) 2011-04-15 2014-07-01 CellAegis Devices Inc. System for performing remote ischemic conditioning
USD708338S1 (en) 2012-08-15 2014-07-01 CellAegis Devices Inc. Cuff for remote ischemic conditioning
US8863325B1 (en) 2012-02-01 2014-10-21 Naum Fiterson Undulating bed
US10179261B2 (en) 2015-04-03 2019-01-15 Better Standing Company, Inc. Standing step trainer
US10213206B2 (en) 2013-03-15 2019-02-26 CellAegis Devices Inc. Gas powered system for performing remote ischemic conditioning
US10797524B2 (en) 2017-10-24 2020-10-06 Stryker Corporation Techniques for power transfer through wheels of a patient support apparatus
US10910888B2 (en) 2017-10-24 2021-02-02 Stryker Corporation Power transfer system with patient transport apparatus and power transfer device to transfer power to the patient transport apparatus
US10966539B2 (en) * 2019-06-11 2021-04-06 Ko-Po Chen Reciprocating device
US11139666B2 (en) 2017-10-24 2021-10-05 Stryker Corporation Energy harvesting and propulsion assistance techniques for a patient support apparatus
US11389357B2 (en) 2017-10-24 2022-07-19 Stryker Corporation Energy storage device management for a patient support apparatus
US11394252B2 (en) 2017-10-24 2022-07-19 Stryker Corporation Power transfer system with patient support apparatus and power transfer device to transfer power to the patient support apparatus

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CN117028448A (zh) * 2023-06-02 2023-11-10 深圳康诺思腾科技有限公司 制动装置

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US20080306563A1 (en) * 2007-06-05 2008-12-11 Jose Roberto Kullok System and method for cardiovascular treatment or training
US8266743B2 (en) 2010-08-23 2012-09-18 Midmark Corporation Examination table with motion tracking
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WO2014055348A1 (en) * 2012-10-04 2014-04-10 Ventaerx, Inc. Methods and apparatuses for increasing mucociliary clearance
US20150272804A1 (en) * 2012-10-04 2015-10-01 Ventaerx, Inc. Methods and apparatuses for increasing mucociliary clearance
US10213206B2 (en) 2013-03-15 2019-02-26 CellAegis Devices Inc. Gas powered system for performing remote ischemic conditioning
US10179261B2 (en) 2015-04-03 2019-01-15 Better Standing Company, Inc. Standing step trainer
US11641135B2 (en) 2017-10-24 2023-05-02 Stryker Corporation Techniques for power transfer through wheels of a patient support apparatus
US11394252B2 (en) 2017-10-24 2022-07-19 Stryker Corporation Power transfer system with patient support apparatus and power transfer device to transfer power to the patient support apparatus
US12350213B2 (en) 2017-10-24 2025-07-08 Stryker Corporation Energy storage device management for a patient support apparatus
US11139666B2 (en) 2017-10-24 2021-10-05 Stryker Corporation Energy harvesting and propulsion assistance techniques for a patient support apparatus
US11245288B2 (en) 2017-10-24 2022-02-08 Stryker Corporation Techniques for power transfer through wheels of a patient support apparatus
US11251663B2 (en) 2017-10-24 2022-02-15 Stryker Corporation Power transfer system with patient transport apparatus and power transfer device to transfer power to the patient transport apparatus
US11389357B2 (en) 2017-10-24 2022-07-19 Stryker Corporation Energy storage device management for a patient support apparatus
US10910888B2 (en) 2017-10-24 2021-02-02 Stryker Corporation Power transfer system with patient transport apparatus and power transfer device to transfer power to the patient transport apparatus
US10797524B2 (en) 2017-10-24 2020-10-06 Stryker Corporation Techniques for power transfer through wheels of a patient support apparatus
US11646609B2 (en) 2017-10-24 2023-05-09 Stryker Corporation Power transfer system with patient transport apparatus and power transfer device to transfer power to the patient transport apparatus
US12029695B2 (en) 2017-10-24 2024-07-09 Stryker Corporation Energy storage device management for a patient support apparatus
US12062927B2 (en) 2017-10-24 2024-08-13 Stryker Corporation Power transfer system with patient support apparatus and power transfer device to transfer power to the patient support apparatus
US12261462B2 (en) 2017-10-24 2025-03-25 Stryker Corporation Power transfer system with patient transport apparatus and power transfer device to transfer power to the patient transport apparatus
US10966539B2 (en) * 2019-06-11 2021-04-06 Ko-Po Chen Reciprocating device

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CA2534302A1 (en) 2005-02-24
US20060185083A1 (en) 2006-08-24

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